In addition to their wide expression throughout the brain, CRH receptors are found in a number of peripheral sites, including the adrenal medulla, prostate, gut, spleen, liver, kidney and testis. Two distinct CRH receptor subtypes have been identified in humans, i.
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Abstract The regulation of brain temperature is largely dependent on the metabolic activity of brain tissue and remains complex. In intensive care clinical practice, the continuous monitoring of core temperature in patients with brain injury is currently highly recommended.
After major brain injury, brain temperature is often higher than and can vary independently of systemic temperature. It has been shown that in cases of brain injury, the brain is extremely sensitive and vulnerable to small variations in temperature.
The prevention of fever has been proposed as a therapeutic tool to limit neuronal injury. However, temperature control after traumatic brain injury, subarachnoid hemorrhage, or stroke can be challenging.
Furthermore, fever may also have beneficial effects, especially in cases involving infections. While therapeutic hypothermia has shown beneficial effects in animal models, its use is still debated in clinical practice. This paper aims to describe the physiology and pathophysiology of changes in brain temperature after brain injury and to study the effects of controlling brain temperature after such injury.
Introduction Many popular figures of speech connect brain activity with temperature. It is now well known that, while brain temperature is largely dependent on the metabolic activity of brain tissue, the regulation of these two parameters is complex.
The relationship between temperature and metabolism is always interactive. While brain cell metabolism is a major determinant of brain temperature, minor changes in brain temperature can result in significant changes in neural cell metabolism and therefore in brain function.
Tight control of brain temperature is critical for optimal brain function under different physiological conditions such as intense physical activity or complete rest. In intensive care clinical practice, continuous monitoring of core temperature in patients with brain injury is highly recommended [ 1 ].
It has been shown that, in cases of trauma, the brain is extremely sensitive and vulnerable to small temperature variations. Indeed, fever is considered a secondary injury to the brain in neurosurgical patients with severe traumatic brain injury [ 2 ], subarachnoid hemorrhage [ 3 ], or stroke [ 4 ], in whom hyperthermia is a frequent phenomenon.
In these cases, guided, directed normothermia can be used to limit secondary brain injury. This paper aims to describe the physiology and pathophysiology associated with changes in brain temperature, with particular focus on acutely ill patients suffering from severe traumatic brain injury, stroke, or subarachnoid hemorrhage.
Physiology of Brain Temperature Energy production in humans derives from glucose, protein, and fat metabolism. The end products of aerobic metabolism are carbon dioxide CO2 and water.
The production of adenosine triphosphate ATPthe main intracellular energy storage molecule, is accompanied by heat Figure 1. The combustion of glucose and protein produces 4.
Heat production depends, therefore, on energy metabolism [ 5 ]. Heat production during energy metabolism. This schema is valid whatever the cell type.
Even at rest, the metabolic activity of brain tissue is high. Under normal conditions, production of heat within the brain is balanced by its dissipation. In contrast to other organs such as muscles, the heat produced within the brain is not easily dispersed due to the protection of the brain by the skull.
Brain temperature depends primarily on three factors: Dissipation of generated heat is improved by vascular anatomical specializations that permit heat exchange. Heat Exchangers Heat exchangers vary across species.
In felids, arterial blood for the brain flows through a vascular network at the base of the skull. In these species, the carotid artery is very close to the cavernous or pterygoid sinus, which receives cool blood from the mucosal surfaces of the nose. This heat exchange produces selective brain cooling SBC that depends on sympathetic activity [ 6 ].
In canids, the carotid rete is rudimentary [ 7 ]. However, the large surface of the cavernous sinus, which is in close contact with the base of the brain, allows direct cooling of the rostral brain stem. Similar regional SBC has been found in other mammals.
In humans, the face and the mucosal surfaces of the nose, which are sources of cool venous blood, are small in relation to the mass of the brain.
Moreover, a specialized heat exchanger similar to the carotid rete does not exist in humans, and a substantial fraction of the blood supply to the brain is provided by the vertebral arteries, which have no direct contact with cool venous blood [ 6 ].
Cool blood from the skin of the head can flow into the cranium and cool the brain via the emissary veins of the temporal and parietal bones [ 8 ]. Moreover, brain cortical arteries can cover distances of 15 to 20 cm in fissures and sulci on the brain surface before reaching their final destinations in the cortex and adjacent white matter [ 9 ].The regulation of brain temperature is largely dependent on the metabolic activity of brain tissue and remains complex.
In intensive care clinical practice, the continuous monitoring of core temperature in patients with brain injury is currently highly recommended. After major brain injury, brain temperature is often higher than and can vary independently of systemic temperature. Textbook in. Medical Physiology and Pathophysiology.
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